Obstructive Sleep Apnea with Severe Chronic Airflow Limitation: Comparison of Hypercapnic and Eucapnic Patients

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Abstract
The mechanism of sustained awake hypercapnia in the obstructive sleep apnea syndrome (OSA) is unknown. Recent work has implicated coexisting chronic airflow limitation (CAL) as an important contributing factor. We approached this question by studying consecutive patients with both OSA syndrome and severe CAL in detail and comparing those with and without retention of CO2 while awake. Of 28 patients with both severe OSA (mean NREM apnea index = 48 .+-. 9, SEM) and severe CAL (mean FEV1 = 1.07 .+-. 0.07 L), 14 had persistent awake hypercapnia (mean PaCO2 = 50 .+-. 1 mm Hg), and 14 were normocapnic (mean PaCO2 = 40 .+-. 1 mm Hg). When separated according to their PaCO2 level, there was no different in the apnea indices in both non-rapid-eye-movement (NREM) sleep, or rapid-eye-movement (REM) sleep, although the hypercapnic group had lower average levels of oxyhemoglobin saturation in both NREM (SaO2 = 77 .+-. 2% versus 85 .+-. 3%, p < 0.05) and REM (SaO2 = 60 .+-. 4% versus 82 .+-. 3%, p < 0.001) sleep. The mean values for FEV1, VC, lung volumes, and diffusing capacity for CO measured while awake did not differ. The hypercapnic group had lower awake PaO2 levels (p < 0.001), were heavier (p < 0.05), had narrower upper airway size on CT scan measurements (p < 0.01), and gave a history of much heavier alcohol intake (p < 0.05). Our results demonstrate that some patients with severe OSA and severe CAL can maintain normal awake arterial CO2 levels. We suggest that depressed respiratory drive is also present in patients with lung disease and sleep apnea who develop hypercapnia. Protracted, heavy alcohol intake may be an important mechanism causing depressed respiratory drive that results in hypercapnic respiratory failure in patients with severe OSA with CAL.